Evidence map›Paper›PMID 21888767›Full record

ArticleRedox report : communications in free radical research2011

Aminoguanidine and N-acetyl-cysteine supress oxidative and nitrosative stress in EAE rat brains.

Srdjan Ljubisavljevic, Ivana Stojanovic, Dusica Pavlovic, Dusan Sokolovic, Ivana Stevanovic

Abstract read
In one paragraph

Article in Redox report : communications in free radical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Excitotoxins, Mitochondrial and Redox Disturbances in Multiple Sclerosis.International journal of molecular sciences · 2017
    Review
  17. Article
  18. Lipopolysaccharide Binding Protein and Oxidative Stress in a Multiple Sclerosis Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Srdjan LjubisavljevicClinic of Neurology, University Clinical Centre of Nis, Nis, Serbia. srljub@gmail.com
Ivana Stojanovic
Dusica Pavlovic
Dusan Sokolovic
Ivana Stevanovic
University of Nis · RSMilitary Medical Academy · RS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a well-established animal model of human multiple sclerosis (MS). We have evaluated the role of oxidative and nitrosative stress, as the causal factors in the development of EAE, responsible for the damage of cardinal cellular components, such as lipids, proteins and nucleic acids, resulting in demyelination, axonal damage, and neuronal death. EAE was induced in female Sprague-Dawley rats, 3 months old (300±20 g), by immunization with myelin basic protein in combination with Complete Freund's adjuvant (CFA). The animals were divided into seven groups: control, EAE, CFA, EAE+aminoguanidine (AG), AG, EAE+N-acetyl-L-cysteine (NAC) and NAC. The animals were sacrificed 15 days after EAE induction, and the levels of nitrosative and oxidative stress were determined in 10% homogenate of the whole encephalitic mass. In EAE rats, brain NO production and MDA level were significantly increased (P<0.001) compared to the control values, whereas AG and NAC treatment decreased both parameters in EAE rats compared to EAE group (P<0.001). Glutathione (GSH) was reduced (P<0.001) in EAE rats in comparison with the control and CFA groups, but increased in EAE+AG and EAE+NAC group compared to the EAE group (P<0.01). Superoxide dismutase (SOD) activity was significantly decreased (P<0.001) in the EAE group compared to all other experimental groups. The clinical expression of EAE was significantly decreased (P<0.05) in the EAE groups treated with AG and NAC compared to EAE rats, during disease development. The obtained results prove an important role of oxidative and nitrosative stress in the pathogenesis of EAE, whereas AG and NAC protective effects offer new possibilities for a modified combined approach in MS therapy.

Indexed as

AcetylcysteineAnimalsBrainEncephalomyelitis, Autoimmune, ExperimentalFemaleFreund's AdjuvantGlutathioneGuanidinesMalondialdehydeNitric OxideOxidation-ReductionOxidative StressRatsRats, Sprague-DawleySuperoxide DismutaseAcetylcysteineFreund's AdjuvantGlutathioneGuanidinesMalondialdehydeNitric OxidepimagedineSuperoxide Dismutase

Identifiers

PMID21888767
PMCPMC6837682
OpenAlexW2156800652

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.